Now Tom starts out misrepresenting things by picturing a fat mouse, likely an ob/ob. This study actually involved females of the strain pictured below:

Kind of a cute little critter, no? The study was also conducted in the context of calorie restriction and its demonstrated increase in longevity of mice. They are not a mutant strain genetically predisposed to obesity.

These mice can live almost 3 years and average about half that. So the two experiments were conducted during normal growth (4 weeks for 8 week old mice in one study, 3 weeks for 10 week old mice in the other). The mice were not made obese then put on a calorie restricted diet. Both groups of mice grew slightly or not at all during the studies. So this study was NOT looking at weight loss in the obese, it was looking at the effect of restricting calories in a normal mouse and testing the response. Now reproductively these mice were adults, but these mice continue to grow throughout their lives. So this might be somewhat akin to putting normal weight young children on calorie restricted diets and seeing what happens. The results may well hold a clue to those impoverished cultures with high rates of true undernutrition in childhood leading paradoxically to obesity in adulthood, but that's not what CDS sufferers see.

Now, before I continue on to discuss this study and its implications, I simply can't help but point out that the last link in the previous paragraph is to a study entitled The High-Fat Diet–Fed Mouse. In this study they fed this very same strain of mouse the usual (11%) fat chow and a high (58%) fat diet. The regular diet was quite high carb (63%) while the high fat diet was fairly low carb (~25%). The results: "Body weight was higher in mice fed the high-fat diet already after the ﬁrst week, due to higher dietary intake in combination with lower metabolic efﬁciency." Why did these mice ACTUALLY *get fat*? They ate more! Someone ought to write a book on this stuff. (I guess Marta forgot to turn up their thermostats and get those futile cycles spinnin, but I digress ...) Something else happened to the fattening mice, they became hyperglycemic, hyperinsulinemic, and had impaired glucose tolerance. This sounds to me like mice overeating on a high fat diet getting obese and diabetic while those eating low fat/high carb diets maintain proper energy balance for normal growth and metabolic regulation to me. Oh wait ... that can't be right! Yeah, I forgot ... this is a mouse study and therefore has no relevance to humans after all. Phew! Explained that one away nicely. Nothing to see here folks, let's move on ...

Sorry, but before we do, let's summarize: This mouse grows relatively insignificantly in mass over the span of 3-4 weeks when fed a low fat - high carb diet in either ad libitum or calorie restricted fashion. With CR, the metabolism slows so that these mice divert more intake towards fat stores than lean mass. The very same strain of mouse fed a relatively low carb high fat diet gets fatter and heavier because the mice eat more.

OK ... So back to the original study, thermodynamics, etc. All of the mice were acclimated to eating ad libitum (AL) throughout their lives up to the start of the study. There were two study "legs":

II: 10 week old mice divided into 2 groups AL v. CR for three weeks. Total fat mass, distribution between various fat depots, resting energy and total energy expenditures (REE,TEE) were measured.

In Study I, both groups increased body weight slightly and similarly. But the AL added more lean mass while the CR added more fat mass. The result reporting as percents is a bit misleading IMO. Note that we're talking mice that weighed around 20g. After 4 weeks the CR mice had 3.37 ± 0.23 g fat mass vs. 2.00 ± 0.09 g. So while the CR group added 68% more fat mass, we're talking 1.37 g of a 20 g mouse - e.g. a redistribution of <7% bodyweight in a period. I also note the variability for the CR mice is quite a bit higher than that for the AL mice indicating that some of the CR mice faired differently than others.

OK, so the CR mice got fatt-I-er, but not "fatter", hence the title of this blog post. The CR mice accumulated more fat tissue compared to the AL mice, and added less lean mass, but, they didn't gain more weight. In other words, they did not become obese. This is important because if we're talking "Why We Get Fat" and saying that it's all about dysregulated fat that accumulates lipid, this study simply does not support such a thesis.

For the overweight ladies in the audience (since this study was in females) who became so in adulthood, think now about how you got fat for a moment. Did you start out a 130 lb woman (or whatever "normal" is for your height/build) with 20-25% body fat and start noticing that despite weighing 130 lb week in and week out for a period of years you started turning to goo and found yourself with 50% body fat? Of course not. When we get fatter, we see the weight on the scale increase week in and week out as we become, say, a 180 lb woman. Does that mean each of us gained 50 lbs of fat? Of course not. I discussed this HERE.

Back to the study, in Part II, they measured energy expenditure and lo and behold TFLOT holds up pretty well. In this part of the study, both groups of mice were relatively weight stable for three weeks. The 5% CR corresponded to a 5% reduction in TEE and both groups were thus in energy balance. The resting energy expenditure (REE) dropped 20% (from 6.09 to 4.83 kcal/day, a difference of 1.26 kcal/day) while total energy expenditure dropped 5% (from 8.38 to 7.97 kcal/day, a difference of 0.41 kcal/day). For the AL mice REE/TEE was ~73% while it was only ~61% of the CR group. Doing the math, the other energy expenditures in the CR group must have gone up even though it wasn't noticeable with the locomotive activity or BAT (brown adipose tissue) thermogenesis (although they didn't measure body temp, rather UCP activity so it is possible that there was temperature compensation not related to BAT). Seems the mice were conserving energy by lowering the "idle" on the engine, all the while expending a bit more on something - could that be the mouse equivalent of fidgeting or other nervous behavior resulting from sensing minor starvation? Who knows. But, the mice that accumulated the most fat also expended a greater proportion of their intake on something other than basal metabolism.

So, where does this leave us in the end? Well, we do know that a certain level of body fat does seem to improve survival rates for disease and injury (sorry no handy reference at the moment). Perhaps CR, by causing the mice to be more efficient at storing energy and putting a bit less into bone/muscle/organ growth end up with bodies that require fewer calories to maintain later in life and allow for sufficient reserves to get through harder times. Makes sense to me. I'm being repetitive, but it is important to note: they did NOT become obese or even fat. The mouse's organs and systems were not strained by managing a significantly heavier body. Even on a small mouse, about one and a third gram is just not a lot of fat spread around several depots - that's like 1/4th of one teaspoon of butter.

OK, so how does this translate to humans, weight gain and weight loss? Well, firstly, when we get fat we GAIN weight. We don't just start redistributing lean and fat mass. And what of losing weight. Isn't that 5% change in TEE in response to a 5% CR proof that the body is adaptable so, that whole 100 cal/day = 10 lbs in a year is totally wrong? Well, for this we could go on and on with the rodent studies, OR, we could acknowledge that we have a crap load of data for what happens to actual humans who are already over-fat and look at that to see if there's really much to be learned here. From the discussion in this very paper we have the following:

A growing body of literature has demonstrated that moderate or severe CR (30–60%) leads to significant changes in body composition including reduced body fat mass and/or lean mass, with or without weight loss (4–6,22,23). For example, 25% CR in humans resulted in a clear decline of body fat mass and fat-free mass after 6 months (5). In 6-month-old mice, 55% CR resulted in a 71% reduction in total fat mass after 6 months (22).

Let us also keep in mind the metabolic rates vs. body masses for various mammals as well. The energy expenditure:body weight ratio is substantially higher for mice than humans. See, for example, the graphic below:

Considering that body temp maintenance is a major component of REE, the mice seem to have a disproportionately large ability to conserve energy as compared to, for example, us humans, because it's a bigger "cost" per unit mass for them.

Here is just one study that quantified both REE and TDEE for actual free-living humans (as luck would have it obese women), that I've blogged on previously. The study looked at LC vs. LF diets and EX (3X 45 min moderate cardio) vs. NX (no exercise) by comparing 4 groups of dieters. The changes in body composition, REE and even TEF did not differ between the two diet groups. For both diets, REE was reduced by ~130 cal/day. This is GOING to happen folks! IF you are losing weight without changing activity, you are in caloric deficit from eating less. Even TEF wasn't different - I've long suspected that this is because the Atwater factors represent metabolizable energy that seems to have been partially if not fully adjusted for the "cost" of extracting the energy.

What influenced body composition most? The much maligned slogging cardio. Yeah, 3X 45 minutes of 15 minute sessions on one of three cardio machines. From the discussion:

More important than total weight losses [of which LC were slightly more than LF], however, are the relative changes in FFM and FM. Exercise training was a major determinant of the changes in body composition, with FM comprising 89.4% of the weight loss in the Ex group, compared with only 71.3% in the Nx group.

So much for exercise being useless for fat loss, but I digress ... In any case, the exercisers had their intake matched to approximate the caloric cost of the exercise itself so that the "calculated" caloric deficit would be the same for both groups: e.g. they got to eat a bit more. But let's look at TDEE:

Directly due to Exercise: EX: +0.07 ± 1.23 NX: -1.46 ± 1.04 MJ/d

Not attributable to Exercise: EX: +0.75 ± 1.06 NX: -0.61 ± 1.03 MJ/d

As I've stated before, I'm not sure these are additive, but +0.82 MJ vs -2.07 MJ between the two. This is a swing of almost 3 MJ or ~ 700 calories!! The result is that the exercisers lost 2.7 kg more on average (that's almost 6 pounds) of FAT. And why? Because they actually increased TDEE from baseline rather than reducing it. And not just from the exercise, but because NEAT (non-exercise activity thermogenesis) increased. So much for the theory that exercisers just lounge around on couches more the rest of the day to compensate. But again, I digress ...

If there is a real lesson to be learned here folks, it is that we should strive for our children to eat a diet that allows them to grow normally and remain lean eating ad libitum, because once we get fat, it's a minefield out there what to do about it. And if we find ourselves as overweight adults, there's no easy fix. We gain and lose both lean and fat mass and we have limited control over it. When we lose weight, TDEE goes down in part because REE decreases (and stays there for the most part) but NEAT goes down too. Exercising can help counter this.

93 comments:

I am not sure why you say, that Tom tries to counter calorie-based theories, because right in the first paragraphs he says

Quote "That second part of that sentence ["ingest fewer calories than calories expended in a day"] is, of course, correct."

He also doesn't seem to deny that weight loss or gain is strictly related to eating/moving patterns:

Quote: "Yup … if you get fat, by gosh, it means you’re either eating more or moving less."

His point is how little relevance a certain physical law has in obesity research and weight/fat regulation. I don't think that he would argue that any of the actual study outcomes (changes of fat, weight, REE, TEE, NEAT in the mice) have necessarily the same or even similar implications in humans. But that wasn't his point to begin with.

He also doesn't seem to deny that weight loss or gain is strictly related to eating/moving patterns:

Quote: "Yup … if you get fat, by gosh, it means you’re either eating more or moving less."

Umm... that would be Fat Head mocking Jillian Michaels because lord knows she didn't get the midriff in an ad that occasionally graces his blog of late because she knows a thing or two about weight loss. Guess it makes these two big men feel a bit more impo'tant putting her down rather than putting forth some sort of consistent theory. She must have hurt his feelings or something: http://www.youtube.com/watch?v=5LNH0RPXI0M

Naughton like his teacher can't spin his way t a consistent explanation because TFLOT and the carb/insulin magical fattening macro/hormone theories don't mix.

To your last sentence: Actually I would say, TFLOT and carb/insulin magical fattening theory are two non-related "issues" - while the former is always right but meaningless, the latter can or cannot be right but certainly without being magical - but we've been over this ;).

You know, I used to think paleo/low carb people were more science oriented. That is, knew junk science when they see it and they do, but only when it is an oppossing viewpoint. Otherwise, what they accuse low-fat, high-carb research of (i.e. transposing mice models to humans, causation/correlation, epidemiology, etc)they are quick to overlook if the research supports their views.

TFLOT meaningless? Good luck trying to perpetuate that 'fact'.On a related note, I've staid shy of 1800 cals a day since october, eating primarly protein and carbohydrate (berries, fruit, lean cuts of meat and a whole lot of wholegrain bread and oats, vegetables and lowfat cheese). I'm currently down 37 lbs.

Yeah, well the only "meaningful" thing you can squeeze out of that law concerning weight regulation is that weight gain is always accompanied by a positive caloric balance and weight loss by a negative caloric balance. Thats about it.

Ok, didn't mean to be so snide, but thanks for the clarification. It's not really that high carb though, just about 150-250 grams a day. It's mostly about getting enough protein while still staying below 1800 kcals :) Also, a bunch of resistance training and ever-so-boring cardio.

Hi King and Welcome! I have to chuckle b/c at 150-250g/day you do realize you are in the "insidious weight gain" zone on Mark Sisson's carbohydrate curve >:) LOL!!

@Christian: TFLOT doesn't need to indicate direction of causality, but it explains perfectly well why surpluses leads to gains and deficits to losses. Ultimately you put too much or not enough food in your body to meet needs, signalling telling you to do so is part of what makes us living beings, but it never goes in reverse. Or are you aware of some humans for whom urine, CO2 and feces are pumped backwards through through their bodies and a steak with a side of spinach, roasted potatoes and a glass of wine and some oxygen comes out of their mouths?

Hi Christopher, NEAT is, by definition, an all inclusive term for any activity that is not "exercise". In the study I quoted in this post, exercising apparently did increase NEAT, not decrease it as some suggest we do in compensation for deliberate exercise. So being active does, at least for some, lead to an autonomous increase in activity overall. Anecdotally I do find myself being more active when I'm exercising regularly. In the end I don't think it matters whether it is intentional or not. AT = moving more does help. I still don't formally exercise, and recent family demands on my time have pushed that down the priority list once again. BUT, I am very active between shoveling snow, shuttling firewood to the house and that sort of thing. I regularly run up stairs in the home, park far from my destinations at stores, etc. It ALL adds up. At least doing this I have had no trouble maintaining of late.

That's part of what I was getting at with NEAT as fidgeting carries over into exercise, i.e. you're going to be more fidgety when you exercise or, as Taubes puts it, Lance Armstrong isn't thin because he exercises, he exercises because he's thin, or rather the propensity toward a higher NEAT informs his desire to move and keep moving at high intensities.

Reverse means cause and effect are switched, not time going backwards. I gave an example before, not sure if you read that:

"Say two identical twins eat two different, yet isocaloric meals both worth, say, 300 kcal. Lets assume over a 3 hour period the metabolic rate of those twins requires precisely 300 kcal. Twin 1 who eats a healthy diet partitions the energy perfectly, leaving the body with the same amount of fat and other energy stores at 3-hour baseline. The other twin however eats a bad diet: 50 kcal of his meal are partitioned into fat storage, the energy difference is replaced by, say, glycogen. So at 3-hour baseline, the second twin is both 50kcal “fatter” and slightly glycogen depleted. Somehow the body senses the glycogen depletion and is signalling slight hunger. Twin number 2 eats an apple worth 50kcal. And boom - thats why we get fat ;)."

Yeah the metabolic pathsways and numbers are invented - i honestly don't care ;). The thing is in this situation - without violating energy balance - the second twin overate because he was getting fatter, not the other way around. You could also say shitty energy partitioning or wrong settling point because of shitty diet. It is perfectly possible for "overeating" to be an effect rather than a cause. At least physics doesn't forbid that.

@ChristianThere's no evidence of any kind that a "bad diet" would lead to more calories partitioned as fat storage. No proof of any kind that certain foods are more conductive to fait gain, not even marshmallows, as long as the caloric intake itself is not conductive to fat gain. And no proof of any kind that certain foods, not even top sirloin and spinach, are less conductive to fat gain, as long as the caloric intake is conductive to fat gain instead.

So there's no evidence that regardless of calorie intake certain foods are more likely to be stored. But even if they were, fat storage per se is meaningless because it is ungoing process. The only thing that matters is fat balance at the end of the day (or the week) meaning fat stored vs. fat mobilized and the only thing that controls this process is your caloric intake vs. your caloric expenditure.

@Christopher: My hubby has one of those friends who can eat an enormous amount of food and remains thin. I've noticed, however, that he sure does fidget a lot in conjunction with his high physical activity (he walks a lot b/c he doesn't have a car or license for one thing, and then there's his job). In the end I don't really care which causes which, although I was a tomboy and a jock and if Taubes is right that was because I was lean not that I stayed lean because I was a jock. So I guess he can explain to me how my jock gene got turned off or something. LOL.

I don't think we can do much about the fidget stuff, but we can do other little things. Y'know initially I did it consciously. Now it's like auto pilot for me.

@Danny- there exists of variety of studies demonstrating that isocaloric diets do affect weight loss and body composition differently based on their macronutrient ratio. This must be the case when one considers the thermic effect of food and other factors like differing hormonal response to different macronutrients entering the stomach and small intestine. Ingestion of protein and its subsequent metabolism is a much more energy intensive endeavor than that of CHO or fat, and indeed, some estimates state that up to 30% of the calories of an all-protein meal are used strictly for its processing. I honestly don't think this number could be that far off the mark considering that ingestion of just 20-30g of protein causes a burst of protein synthesis in the body for a couple hours following.

@kdsprotein is the only variable.Isocaloric diets that are inadequate in proteins are worse for weight loss. Isocaloric diets that are adequate in proteins are not worse for fat loss than diets that are higher in proteins and the ratio of fat to carbohydrates is irrelevant as long as the diet is isocaloric.

@kds: Young (referenced by Mannimen) is really one of the worst studies I've ever seen. James Krieger, as any good scientist would do, has since revised his conclusions based on new/re-evaluated evidence controlling for protein. No one disputes that protein is a bit "special" in a way, though I do think Atwater factors already account for part of this.

@Christian: Please think about the evolutionary consequences of what you (and Taubes) propose. Isn't the whole point of fat cells to store energy in times of plenty so we can survive through times of scarcity? But according to you, when a hunter gatherer killed a large fat animal and had plenty of fat and calories for dinner, their body would not store any of those excess calories, because the meal was zero carb. When the hunter gatherer didn't manage to hunt anything and had to survive eating roots and vegetables and fruits, who are fibrous and poor sources of calories, their fat cells would not release any energy. It was like having a bank account that doesn't let you put money into it when you have plenty and doesn't let you withdraw money when you need it. Does that make sense to you? Do you honestly believe that was what happened? Please tell me how humankind manage to survive to this day.

@CarbSane: I didn't know about Sisson's weight curve, but I googled it now. That's pretty funny. About half of my carbs comes from fructose (I eat bananas, apples, raspberries, blueberries, strawberries and currants daily), which I guess should compound my problems. I also make juices of apples, carrots and the like.

I also take one day a week where I eat 300-400 grams of carbohydrate, to increase leptin. Wholegrain bread with honey. Delicious :)

It sounds easy, but it's literally taken me years to really get the groove going (six years ago I weighed 330 lbs, today I weigh just above 200). What got me fat was never carbs in the first place. It was the overconsumption of calories, in the form of burgers, pizza, chips, cookies, chocolate and stuff like that. I don't eat any of that stuff any more (just the occasional slice of pizza and the occasional burger). I made a concious effort to change my diet for good, and it's finally sticking.

A few years ago I gave lowcarb a try for quite a while. It worked, but not any better than having my carbs like I do now, and having to avoid carbs all the time turned into a huge mental chore. In short, I figured it wasn't all it was cracked up to be. Reading the science about how carbs work (I think I've read every post on this blog), makes me realize I was right to bring carbs back into my diet.

@ Mirrorball: Actually evolution is one of the reasons why I toubt the whole carb/insulin story is complete - precisely because of the example you gave. If you hunt down a big fat mammoth after 2 weeks of starvation it just makes no fucking sense that Glucose should be needed to store fat. And please can you distinguish between "my view" and Taubes? I am not saying carbs make us fat - I am pointing out (like Tom in his blog post) that physics do not forbid overeating to be an effect. That's all. And if it isn't prohibited a priori, then it is worthwhile thinking about it - at least that is my point of view. Even if you make stuff up ;)

"There's no evidence of any kind that a "bad diet" would lead to more calories partitioned as fat storage."

Well, if that really is so then case closed. But again - physics can't tell, only "evidence". And btw if you ever read a book about nutrition for weight lifters (e.g. by Lyle McDonald) you would know that this is precisely what these people are mostly occupied with: energy partitioning aka when can I eat how much of what that it goes to my muscles and not to my hips.

And a last point: Yes, if you adjust for caloric intake this discussion about macronutrients might all have little relevance. But if you don't and just eat till full, wait till hungry again and repeat - then this might become relevant.

@Christian: If you eat more than your body requires, then yes it matters what you're eating. What you eat today, walks tomorrow. The thing is, when talking about fat storage, nothing matters until you're in a caloric surplus. When talking about health, everything matters. You can loose weight and bodyfat if all you're eating is 1000 kcals of chocolate every day. You're not going to enjoy a long life though.

As for Lyle's books, keep in mind that the methods you're thinking of when referring to him are the cyclic diets that are meant to let you lose weight while sparing muscle (or UD2, which is total glycogen depletion followed by a massive carbup). For muscle gain, Lyle has specifically said that the best course of action is to cycle between a modest calorie excess for a period of time, and then diet off the fat that accompanies muscle gain. Remember, Lyle is concentrating on the guys that have very little bodyfat. For those people, losing bodyfat without losing muscle is a big struggle. For the rest of us, these things are overkill.

Whatever you eat, the body will handle. What it won't do is flush out food undigested, which is the only way calories from food would be made unavailable to the body.

And btw if you ever read a book about nutrition for weight lifters (e.g. by Lyle McDonald) you would know that this is precisely what these people are mostly occupied with: energy partitioning aka when can I eat how much of what that it goes to my muscles and not to my hips.

Yes but that's because they are on hypercaloric eating and when you are eating 2000 calories more to gain weight you need to make sure the excess is not used as energy to store but as energy to build muscles. And most weight lifters screw it up anyway because they eat more energ than their body needs to build muscles since muscle growth is limited by protein synthesis and they become fat anyway, although it's concealed by bigger muscles.

@Christian: I think perhaps we're on two different tracks here. Let me try once more to explain my position. What Tom seems to be trying to do with this post is essentially say that the carb/insulin hypothesis is feasible because this study showed the mice got fat on a calorie restricted diet. But the problem with this is that they didn't get fat! Taubes' theory is flawed because even a very high carb diet will not elicit "excessive" insulin unless it is chronically hypercaloric. The pp insulin spikes aren't what control the 24 hour cycle of release of fatty acids from the tissues, and basal insulin is going to remain normal. Let's forget the "pre-existing" 2-3% of humans that seem predisposed to obesity and exist in every culture on every diet, because that goes nowhere to explain the epidemic. The rest of the obese, the climbing rates, are not explained by fat cells "going rogue" (as one Taubes fan is now claiming) and post prandial insulin trapping fat in the fat tissue so it's not available to be used for energy. This is what Taubes claims causes us to get fat - fat accumulation -> over-eating.

There may be clues in this study that explain obesity in adults in impoverished cultures. Topic for another post.

BTW: I can't get Tom's response as he has not published the couple of comments I made on that thread. Apparently reading his blog and commenting politely a few times in response to his comments on my blog is "stalking" to someone with a bloated head.

Excellent comment! I don't think anyone questions that our bodies have compensatory mechanisms, but there's no evidence for carbs causing our bodies to starve our lean tissue in favor of accumulating fat. This study might seem to imply this, but it seems that restriction during growth does cause an animal to put a bit less into growing bigger and a bit more into reserves. The generation that grew up during WWII with rations, etc., is filled with examples of stunted growth.

@King: CONGRATS on that weight loss. Slow but steady progress and maintenance is better than riding the wild rollercoaster. I can't change the past, but one thing I hope comes of this blog (and why I share personal stuff in the other one), is to perhaps save some others from having to go through it.

The LC community, unfortunately, seems to ridicule those who are successful with the conventional approach. LOTS of them out there. Why is this? Because you don't fit the rebel mode and the theories. They are not content to promote low carbing as another, healthy, possible solution to the problem. Most people cannot live on consistently <20g carb/day and what do you tell the rest? What do you tell those who do not lose on low carb diets? These people get accused of not really doing low carb the right way, and now they're being told that they may be so carb sensitive they can't tolerate leafy greens.

Dr. Dansinger reported in an interview with Jimmy that about 1/3rd of The Biggest Loser contestants keep all the weight off, another 1/3 gain back about half, and the rest gain it all back. In the overall scheme of things, that's a pretty good track record.

"What Tom seems to be trying to do with this post is essentially say that the carb/insulin hypothesis is feasible because this study showed the mice got fat on a calorie restricted diet. But the problem with this is that they didn't get fat!"

Hmm, if you think so. But as far as I can tell Tom mentions neither carbs nor insulin in his post and it was actually not about strengthening Taubes insulin theory. It was about the simple fact, that if (<- you notice the big "if" there, right?) is true, it would not violate any laws of physics. A subtle point, that makes all the difference but is somehow difficult to propagate to people who are constantly mixing "the insulin fattening theory" and "the implications of physics for weight regulation". Tom's post was about the latter.

You can pretend that Tom's sum total knowledge of insulin/obesity is based on anything other than what he's read by GT, but his interviews and posts belie otherwise. He is trying to explain thermodynamics in the context of GT's theories because if you have read his discussion on insulin (see Insulin Wars post) he doesn't have to specifically mention carbs/insulin to recognize where he's going with each post. Just as I don't have to repeat each and every belief I have here for regular readers to know where I stand or where I'm going with my work.

He got roped in by the title of the article and the %'s of change in body composition and ran with it. He talked of "fat mice" - they weren't fat - and calorie restriction making you fatter. Mocking Jillian is his way of saying ELMM doesn't work and "here's proof" because CR made these mice "fat". But he neglected to put it in proper context.

I asked him some questions on his blog, but again, he's a-scareded of being "stalked" so he opted to delete the comments.

@Danny: If one takes a gander at Jimmy Moore's menus early 2008 (http://lowcarbmenu.blogspot.com/2008_01_01_archive.html) where he "mysteriously" gained 25 lbs in 6 weeks when he started lifting some weights, you'll see a perfect example of what you're talking about. Of course some would blame hidden carbs in all that product, but he's clearly WAY hypercaloric.

@Danny, I know that protein intake is the X factor and I'm aware from previous posts that CarbSane knows this as well. Forgive me for not knowing that you knew that considering your original post I quoted made no mention of "isoprotein".

Indeed, just as I think GT et al are mistaken in holding to a narrow view of cho/insulin, I think FLOT shouters are equally myopic in ignoring the interplay of insulin/leptin on hypothalamic appetite stimulation as it relates to ad libitum diets. A calorie sure is a calorie, no doubt about it, but "stop shoveling food into your fat face" has not been very effective advice, and it seems to be almost absurd advice when treating 5-6 year olds who become obese even when they have the same access to food and the same physical routines as their lean siblings. I find Lustig's take on insulin/leptin interplay in obese children fascinating (http://www.nature.com/nrendo/journal/v2/n8/full/ncpendmet0220.html).

@CarbSane- do you (or anyone you know) by any chance have access to two of the other studies referenced in the Manninen letter? I would like to see M&M and detailed results of the insulin receptor-knockout mice and intensive insulin therapy weight gain in IDDM studies:

@kds: "stop shoveling food into your fat face" has not been very effective advice

Actually it has been quite effective for those who heed it. When I was obese I ate a lot. I had convinced myself that it wasn't really that much, but it was. Why does the fact that people lose weight eating LC diets because they eat less need some contorted explanation. Sure genetics play a part. I had a friend with 3 boys - two looked like her (she was obese), one looked like the Dad (thin). The former were overweight, the latter rather scrawny, yet they ate the same diet. However they didn't eat the same amount, the fatter boys ate more. They were also cuddlers when "auntie" came over while the thin kid, even when playing video games, was fidgety. I know not how to treat such a situation, but putting them on a low carb "diet" is not likely to be all that much more effective than any other diet.

Sorry can't even find full text link for that first one, LMD found the second one.

Insulin therapy is not analogous to physiological endogenous insulin behavior. As noted in the comments elsewhere, there are different types with different half-lives that are longer than endogenous insulin. Knock-outs are useful to discern pathways, etc.

Postprandial insulin release does not cause hyperinsulinemia unless, I suppose, a person is eating starch and sugar every few hours around the clock. I suggest such a person has other problems besides insulin ;-)

As even Tom pointed out, the results did not counter the bank account model. The model is simplistic but holds up fairly well as an approximation. However, we have limited control over where caloric excesses go (we do add lean mass as well as fat mass) or deficits taken from. Even with adequate protein it seems we still lose some lean mass.

Razwell, nobody here claims to have all the answers as to what causes obesity or how to reverse it in free-living humans. But we DO know HOW we get obese - a consistent positive caloric balance - and HOW, technically, to reverse it. If you lock an obese person up and give them limited access to food, and perhaps only the electricity they can generate on a stationary bike, they will lose weight (fat and lean).

The problem we have is that there's far more to obesity is that there are multiple causes that have nothing to do with energy balance or fat cell regulation and all that. These are the things that lead people to regain the weight. You need to read a bit over at my personal blog to get an idea of where I'm coming from with that. You see, I know I was never genetically programmed to be obese or even overweight, and that there is an epidemic of obesity really cannot be denied. To say that we are on average only like 7 pounds heavier masks the fact that the percent of the population that is 50 lbs overweight has grown considerably. We need to prevent this from happening which means find out what foods cause overeating (and I suggest tasty carb+fats and liquid calories) to begin with, not concocting theories to demonize a macronutrient that helps sustain the human population (eliminate most carbs and there's just not enough of what's left to sustain all of us) with many examples of doing so with impressively low obesity and disease rates and impressive longevity. Then we need to find ways to enable obese people to get into and sustain an energy deficit so as to normalize their weights. That last part is FAR easier said than done. And I might point out that low carb diets seem to have no better track record than any others.

I should word one thing more carefully in that I don't believe foods cause overeating per se, a better wording would be that we need to identify those foods that are more easily consumed in excess. Let's suggest two foods: macadamia nuts and potato chips. Most people will overeat both of these if faced with a giant bowl full and asked to eat until full.

Reverse means cause and effect are switched, not time going backwards. I gave an example before, not sure if you read that:

"Say two identical twins eat two different, yet isocaloric meals both worth, say, 300 kcal. Lets assume over a 3 hour period the metabolic rate of those twins requires precisely 300 kcal. Twin 1 who eats a healthy diet partitions the energy perfectly, leaving the body with the same amount of fat and other energy stores at 3-hour baseline. The other twin however eats a bad diet: 50 kcal of his meal are partitioned into fat storage, the energy difference is replaced by, say, glycogen. So at 3-hour baseline, the second twin is both 50kcal “fatter” and slightly glycogen depleted. Somehow the body senses the glycogen depletion and is signalling slight hunger. Twin number 2 eats an apple worth 50kcal. And boom - thats why we get fat ;)."_______________And at the end of the month you weigh the 2 and the 2nd twin has less fat mass. First law will tell you what to do: go back and find the input or output stream you missed. (you missed that he's a contestant on Biggest Loser & is exercising)

"Insulin makes you fat" will tell you nothing.

First law explains the situation and gives you avenues to troubleshoot. Insulin theory tells you next to nothing (besides being wrong).

I was referring to that statement from a public health/epidemiological perspective. No one disputes that consuming fewer calories than you expend will make you lose weight. This is a ridiculously simple fact, most fat people know this fact while simultaneously not wanting to be fat, and yet obesity/diabetes rates are absolutely absurd. CI/CO is the obvious how, but it says nothing about the why. 'Why' are some able to heed the advice and stop stuffing their faces? Why can some keep off the weight once they lose it yet others seem almost predestined to yo-yo or regain? Why is it near impossible to make some of the folks in this BBC documentary (http://www.youtube.com/watch?v=_6-A0iHSdcA) gain weight and hold on to it permanently even with thousands of calories/day worth of overfeeding?

Portion control, declining physical activity, increased palatability of food, failure of character/ willpower, too many carbs, too much fat, ad inf. are just not satisfying enough answers. I agree with Lustig in that biochemistry drives both metabolism and behavior- I'm just waiting for some well-done primary research that succinctly elucidates some meaningful mechanism(s).

Razwell, I don't know Uribe's problem, but clearly he is one of those *rare* cases where there's probably an underlying metabolic problem. For example, if someone does not properly oxidize fats they'll disproportionately store them and overeat carbs to compensate for energy. This is what they've done to one of those mutant mice or rats, whatever. He still fits the bank account model and follows TFLOT, it's just that there's little hope - other than pharmaceutical/surgical intervention to fix the metabolic problem - he would be able to lose down to a normal weight.

@kds: I got the gist of what you were saying. I agree that just telling folks to eat less has not been an effective approach. But if just telling people to eat fewer carbs were any more effective, the problem would have been largely solved here in the US following the 2003ish Atkins craze. As an adult, I actually don't give a crap how I got obese. We all know for ourselves how that happened. It's how to lose the excess weight and KEEP IT OFF. There ARE lots of people out there who have lost a ton of weight and kept it off for a decade or more. What these folks all have in common is making a PERMANENT lifestyle change. This is simply very hard to do.

Where low carbers are concerned, too many are convinced that all they have to do is cut out the carbs for "effortless" weight loss and maintenance. There's those stories out there of folks who no longer have to watch what they eat and the sky is blue every day. But that is not reality for most. There's this new whiff that if LC only gets you so far, that's the best you can resign yourself that you can do and ever experiencing a hunger pang is akin to torture.

How can we "eat when hungry stop when full" if we never let ourselves experience hunger?

We Americans, especially it seems, have a very bad idea of how much we should be eating and actually are eating. I really think the Starbucks, energy drink, etc. fads are huge culprits in this. When I was a kid we didn't drink with dinner, although most of my friends usually had a glass of milk. I don't remember Mom having a drink in her hand 24/7. She had a cup or two of coffee in the morning, and maybe one in the afternoon. A normal cup, not the huge mugs I have >:) McD's is advertising a caramel mocha coffee thing these days. A medium is almost 300 calories. Just a coffee, with cream and regular sugar would be like half that. And there are people who have these things and chai and whatnot daily. This would have been unheard of in the 70's & 80's. I knew a few soda junkies but few drank regular soda or KoolAid all day long. We drink constantly, even "push" water. I question the wisdom of this, even with non-caloric beverages.

Is it so ridiculous to assume that his problem is just an extreme manifestation of the same or a similar underlying metabolic problem that a growing number of people seem to develop? I am just curious. Do metabolic problems not obey some kind of "gradual progression" or is it always like this man clearly has it and this man doesn't?

No Christian it's not ridiculous, but I would suggest that he had an "extreme predisposition" to have developed such and extreme manifestation.

Where I keep getting tripped up over trying to pin the cause of the obesity epidemic on metabolic dysregulation is twofold:1. Sugar, wheat, refined carbs, potatoes, all manner of junk food to pastries, etc. have all been around long before this epidemic. So have the percentage of those predisposed changed considerably? There is *some* evidence for this being multigenerational relating to fetal nutrition in the womb, birthweight, etc. something I plan to address in coming weeks. But I don't understand why we keep trying to construct elaborate theories when we KNOW folks are eating more. The "why" is not insulin per se from any evidence I've seen.

That the "why" is not answered by carbs or insulin per se is kind of obvious from populations eating high carb / high glycemic without adverse health effects. But I don't expect there to be a simple answer to this problem. But "because they ate more than they expended" can only be a satisfactory answer to someone who is satisfied with tautological answers in general.

OK, one last try: You get fat because you eat more than your body requires. You get leaner because you eat less than your body requires. Nobody ever said TFLOT tells us why some folks require less energy to do seemingly the same things. Nobody ever said TFLOT tells us why we stuff our pie-holes. Or that TFLOT explains why we lose weight because a disease causes us to lose appetite. That list could go on.

Sanjeev put it brilliantly: TFLOT gives us tools to troubleshoot the problem. LC gives us one tool to control intake.

Christian it struck me as brilliant in its simplicity. Maybe it's reminiscent of the engineering approach. We can all go on and on about "why we get fat" and various theories, but here's my bottom line: In 2007 I probably weighed close to 300 lbs if not more. Low carbing my way brought me down to around 210 lbs but then it basically stopped working. I've lost 10-15 pounds since then so yes, you read that right, I weigh somewhere just south of 200, but I'm not large. Looking for answers, TFLOT provides us with options to troubleshoot the situation. Can I simply change diet and impact CO by say TEF? Can I exercise consistently enough to impact CO or increase lean mass while decreasing fat mass to increase CO? Or must I necessarily decrease CI?

When a system is not working, we systematically troubleshoot areas that could be culprits. Does TFLOT offer up all troubleshooting possibilities? No. But looking at TFLOT in that way I though was quite brilliant. Not every brilliant statement must be a ground shattering scientific masterpiece.

Well it is certainly not my intend to insult you or anyone so my apologies if I might have. Concerning your personal weight loss struggle I can just wish you all the best. As far as troubleshooting goes it is still my honest opinion that your knowledge about metabolic regulation will provide more helpful answers and insight than the energy balance equation ever could.

Christian, I think if you read a little more (and I probably have about 20-30 posts that are 90% done from back last summer) around here you will find that I don't focus on TFLOT except when I feel the denial or misrepresentation of physical laws muddies the discussion. Here is where I have seen tens of posts along the lines of (whether he says it exactly in so many words or not or contradicts it elsewhere or not) "Taubes says calories don't count why am I not losing weight" or "I'm doing everything right why am I gaining" and folks wasting months and even years unlearning bad science from GT. You are definitely welcome here (although it appears Tom deleted your posts referencing my blog ;) ), I just don't want to see things devolve to personal attacks. So far this place has been wonderfully easy to manage in that regard and I really hope it can stay that way. So back to the troubleshooting for a moment, if we can fiddle with metabolic regulation to our advantage isn't that the point? But it will only be to our advantage if it impacts some term in TFLOT. Makes sense?

If people eat less on low carb and lose weight, why concoct some alternate explanation for the obvious? But when people don't and they start looking for obscure explanations before addressing the obvious, that leads to frustration and wasted money, time and effort. When I see someone like Jimmy (to whom I have commented several times on his menus blog) frustrated with his weight regain struggles and unable to see the forest for the trees (e.g. when he eats less he loses, when he eats more he does not or he gains) it genuinely saddens me. Folks can believe that or not, but it's the truth.

I am not sure if you really want me to reply to these questions or if I should just shut up ;). I just can't resist because you raise important issues.

1) Calorie denial: I fully support you in so far that many, many people read Taubes first book and got away thinking they could eat all the palatable low/no-carb food in the world and still lose weight. I am convinced that Gary himself thought that at that time (although to a much lesser extend maybe) because of the whole GP-rate-limiting-conjecture. That is not true of course. As Lyle McDonald says you can get shredded on an all carb diet and you can get fat on a no-carb one.

2) Troubleshooting: I think "fiddling with metabolic regulation to our advantage" by means of directly addressing the metabolic pathways in our body that control fat metabolism and hunger signalling is one key player in preventing / curing obesity. The fact that it will - of course - impact a term in TFLOT is trivial.

I read Keith Frayn's Metabolic Regulation. I am not pretending that I understood much of it but the chapter "energy balance and bwr" just upsets me. This guy is literally trapped in his one-way interpretation of thermodynamics which is bizarre to me. I am not proposing that he should do a complete turn-over and suddenly propose that carbs->insulin->obesity or anything like that. But he says that "insulin and leptin are important signals involved in longer-term regulation [of fat depots]". At some other part he does the calculations that a teeny weeny caloric offset is sufficient to explain considerable weight gain or loss over prolonged periods of time. Yet - all he has to offer as a treatment is that we must eat less than we expend (a tautology), that this is difficult to do because we are fighting a massive regulatory system which his whole book is all about and that it is "dispiriting" that long term success with this treatment advice is ineffective at best.

3) That is the reason why I want to have a real explanation for "the obvious". If people lose weight on a low carb diet - it just has to be that they eat less than they expand. I want to know precisely "why". Is it because we ruled out a large proportion of palatable foodstuffs? Is it because they now eat protein and are just more satiated? Is it because we affected the metabolic regulation of the body to their advantage? Is it because of some other reason?"The obvious" can be a sufficient explanation in some cases (maybe Jimmys case belongs to this category) but must not be one in others.

@Christian: Please do keep posting! If things get repetitive I'll just put up the "agree to disagree" flag and we'll move on 8)

Re #2: You're actually hung up on the wrong thing regarding TFLOT and directionality. Taubes has utterly confused this situation by misrepresenting TFLOT. The correct energy balance equation for the process is: Ein = Eout + Estored (alternately Ein - Estored = Eout). This describes the process of energy use. Mathematically you can write Ein - Eout = Estored and then say the right drives the left for some convoluted chapter in a book, but the whole discussion is nonsense. Frayn's treatment is in no way misguided and Taubes' attempts to show it is driven by the right side of an incorrectly arranged equation is a distraction. Regulation is just that - insulin is a traffic cop in the regulation - but we can't make something out of nothing. Taubes proposed causality is that fat starts to accumulate and then you eat more. It's utter nonsense. He does not present any evidence for this and believes it's everybody else's job to prove it wrong. That's not how science works.

As to why most people eat less on low carb it IS the protein. Nitrogen balance is a critical thing that our bodies seek to maintain in the face of varying input. Taubes acts like nobody's been looking at this sort of thing. A quick Google scholar on keywords protein satiety demonstrates otherwise. I've posted a few here, see my protein label. There's also a lot of info out there implicating branch chain amino acids BCAA's, leucine in particular playing a key role.

I don't think there's any one single explanation for why we get fat. Taubes totally ignores any societal/psychological issues and yet I know that's how I ultimately got this way. My husband was a low birthweight premie, so one article I read says he was actually born "fatter" and more susceptible to IR and obesity. So when he got up to almost 300 lbs it would be easy to blame this, when it was because he was out of work,depressed over the death of a loved one, eating a boatload of food and drinking beer. Or maybe it's like so many men I know who can eat a ton and stay thin through their 30's and fail to adjust when their metabolisms start to mysteriously slow down when they reach a certain age. Same for women. Maybe it's because too many of us HAVE gone on a diet at some point and try to micromanage our intake rather than listening to our bodies. There's no single cause, no single macronutrient cause.

Hmm it is hard to argue with anything you just said because I also have seen Taubes presentation and read his book and I also know the shortcomings of his (mis-)representations of things. I therefore totally agree that Taubes understatement regarding any social/psychological/environmental factors is not adequate and/or helpful for this discussion. It also seems evident that there is no single macronutrient cause per se, yes.

My point still remains that Frayn's treatment options are highly misguided. Regulation (or better dysregulation) is "not just that", it could be a crucial key factor here.

@Nige: Note the word "limited". We have some control over it, but ultimately that is limited.

Some people can do any manner of training and just never be able to add much if any muscular bulk. Me? I do. I suppose this is one of my saving graces and something low carb seems to encourage partitioning to lean tissue because most people who don't know me or my weight history peg me at ~150-60 lbs. A bit OT, but you know you've made it when young men (e.g. friends of my hubby) will comment on certain fat women in your presence. It bothered me that they did at first, and I mentioned it to my husband - something like "don't they realize they're insulting me?" - and he said something like "See? They see you as a thin person".

--But if just telling people to eat fewer carbs were any more effective, the problem would have been largely solved here in the US following the 2003ish Atkins craze.--

I think "craze" is quite the apt choice of word. I don't really know how many people made an honest go at a low-carb way of eating back then, but one thing I'm certain of is that "fat makes you fat" was still as much an overwhelming part of the zeitgeist then as it is now. At any rate, I agree that making permanent changes in one's lifestyle is what really matters. Indeed, what does the data say about compliance to a reduced calorie LC vs. reduced calorie LF diet?

--As an adult, I actually don't give a crap how I got obese. We all know for ourselves how that happened.--

As I've been saying, the 'how' (CI/CO) is fairly obvious and mostly irrelevant inasfar as treating the underlying 'why' in the general population. I feel like we're stuck at a root issue of causation,and I believe Taubes is only somewhat off the mark in his simplified analogy regarding fatness preceding overeating. Instead, I think the focus should be on a hypothalamic physiologic/behavioral setpoint. What are your thoughts on leptin/insulin signaling and how it relates to the derangement of this weight setpoint. Stephan's blog series on the topic comes to mind:

I posted on this on another thread, so sorry if I'm sounding repetitive.

While, at an individual level, there are multiple causes for obesity, and while the technical explanation always concurs with TFLOT, I believe the best -catch-all' hypothesis on the 'WHY' question goes like this;

1) Most human beings are largely products of their environment...this is true of moral, aesthetic, and behavioural choices (including eating behaviours). 2) The environment in many developed and developing countries has become increasingly obesogenic (highly palatable foods that are calorie dense and cheap, sweetened and calorie-dense beverages, the rise of the 'food as entertainment' culture, the changing of aesthetic and social norms to accommodate the change of weight norms etc.).3) Human beings have evolved to eat to excess in times of food abundance.

Add these three things together, and I think you get a simple picture of why things are going awry (hopefully the simplicity of the saint, and not the simplicity of the fool).

We haven't got more gluttonous than our forebears; we simply eat more because our environment cues us to do so (i.e. they would have done the same thing had they been transported forward in time; just as indigenous cultures alter eating behaviours when exposed to western 'abundance').

And of course this occurred to me after posting; there are lots of precedents for catastrophes that never materialized.

Here are some of the massive, expensive public scare campaigns that stand out in my memory-

What happened to the "death of the age of antibiotics" and the "return to the bad old days of infectious deseases" I read about in the 80s?

What happened to the "explosive rise" in diabetes that would overwhelm and bankrupt the Canadian health care system by the late 90s?

And of course AIDS was going to kill all of us ... sparing only those who could capture a unicorn.

What happened to the something Taubes himself wrote about, the blood pressure and salt tsunami from the late 70s to the early 90s? Given his history, it surprises me he's never raised the possibility (that I've found) that the obesity epidemic might be a variation of that.

I've always said that if all the fast foods, restaurants, theaters, starbucks and so on started to serve only LC while keeping the prices low, we would have the same rate of obesity. The LC breakfast bowl at Hardees is aroud 1000 calories.

It's food abundance, availability and our drive to overeat when food is abundant that makes getting fatter so easy in the modern times. Food quality or food type has nothing to do with it.

@Sanjeev: I do think there's some truth to the notion that the obesity epidemic is a myth. Now we have our first lady talking about strong arming restaurants into cutting portion sizes and our federal government meddling in school lunches. There's no denying that we're getting fatter however, when there's enough of a market for them that casket manufacturers are mass producing extra sized caskets, and there's no denying there are more and larger plus sized clothing stores/departments. At Kohls and Walmart it seems often that the plus depts are as big as the regular womens size depts.

It's going to get really tricky at some point figuring out how to cover "lifestyle diseases". Many of our states are looking to add sodas to the "sin tax" list ... where does that end? They claim its in a public health interest (like all the ciggy taxes), but it's to raise revenue plain and simple.

@Harry & Leo: Abundance + Convenience + Palatability = Overeating sounds about right. Especially eating out there's something extra about getting a deal. You buy the cup for the soda and get free refills it seems almost wasteful to only drink 8 oz. I really do think our obsession with drinking period - even water - is misguided and obesogenic.

You've mentioned this a few times, and I just don't get it. How can drinking water, even lots of water cause obesity? If it's all about calories then water should make no difference at all since it has none. I've even heard arguments to the contrary: that drinking lots of water can help to curb appetite.

Well, I was trying to find info on drinking water and ghrelin response. I can't find any studies done on over-consumption of water. Water seems to be used as a control because it basically has no effect on ghrelin. However, in my searching I found this study which I thought very interesting.

The nutritional control of ghrelin secretion in humans: the effects of enteral vs. parenteral nutrition.http://www.ncbi.nlm.nih.gov/pubmed/17061019

It's not particularly new so maybe everyone has seen it. They tested the ghrelin response to various "foods" over the course of 3 hours. The only one that significantly reduced ghrelin was glucose. I found it surprising. Just sharing.

Hi MM: I don't know if it "causes" obesity per se, but it certainly can contribute to long term dysregulation of appetite-to-calorie intake in my opinion.

When I was a kid-teenager I was a tom boy-jock. And yet we would line up for a few sips out of a water fountain after lengthy recess/game/practice, etc. I was a babysitter and camp counselor and I do not recall worrying over the kids ever dehydrating. Now? We were descended upon at a hotel pool once by a kids group outing to said pool and after a half hour the coordinator whistles everyone out of the pool for a water break! A bit extreme, but ...

The first time I did the water thing was along with my first diet, because it helps you to feel full thus curb appetite. I think it also helps for the mindless boredom snacking to just have a non-caloric beverage instead. But it is well known that some of our hunger-signalling hormones are secreted simply in response to distension of the stomach. For a while you'll feel full drinking water, but in the long run your brain may begin to associate a level of fullness with a lack of nutrient availability prompting you to need to eat more so as to be even more full to sense satiety. This is just a theory of mine.

There's no evidence for any benefit to water drinking. I take a lesson from my cat. A year and a half ago both were a bit overweight and kitty #1 was looking sick, kitty #2 had stinky poop but was otherwise spritely and the vet was not concerned by anything at his last checkup. Switched them both from quality dry food to canned tuna (cat food version). They got leaner (not lean), one died (#2, age 10) and #1 is still kicking. I avoid gluten in his diet and his allergic skin condition is better (not cured by any stretch). When they ate dry food I had to change water almost daily in their bowl. Now? My kitty is almost never seen drinking water ... he seems to get what he needs from about 1.5 cans of wet food a day.

@Leo"I've always said that if all the fast foods, restaurants, theaters, starbucks and so on started to serve only LC while keeping the prices low, we would have the same rate of obesity. The LC breakfast bowl at Hardees is aroud 1000 calories."

Yeah, except most people who eat a 1000 calorie HP, HF, LC meal like that are satiated for much, much longer than they would be eating a bagel or a donut or a stack of pancakes. I would contend that there isn't a single person described by a metabolic syndrome picture who got that way de novo by eating strictly low carb. The one thing that these people have in common is that their high fat intake is coupled with a high refined carb intake. I think it's clear that many dieting fat people can stall or somewhat reverse their weight loss by consuming too many low carb calories, but I find it near impossible to imagine that someone (otherwise lacking a hypothalamic disorder) would be able to start out lean and later develop diabesity without significant consumption of grain-based desserts, pizza, pasta, french fries, cheeseburgers, and especially sodas and other liquid calories.

but I find it near impossible to imagine that someone (otherwise lacking a hypothalamic disorder) would be able to start out lean and later develop diabesity without significant consumption of grain-based desserts, pizza, pasta, french fries, cheeseburgers, and especially sodas and other liquid calories.

Only because right now pizza, french fried and cheeseburger are the cheap and abundant foods so if you're following a paleo, LC or something diet you're surrouded by forbidden temptation.

But if for any reason LC and paleo foods became the cheap and abundant food that you can buy at any corned of the street, in any fast food, theaters, playground... then it would be the norm for people to become fat eating nothing but LC and paleo foods. That's because way more important than caloric density or type of food is cultural food abudancy.

We're wired to overeat whenever we have a chance to increase our endogeous stores. This means that the lack of processed and caloric dense foods in nature has never been an obstacle to our overeating and fat-gaining needs. Only food availability is.

We've never been as obese as we're today because food has never been this cheap and available. Changing the type of food won't change anything, because the most important, and pretty recent, cause of obesity would still be there: extreme food availaibility and abundance.

Leo- there is abundant evidence to support that ad libitum LC diets are naturally limiting in regard to caloric intake. On the other hand, "people are getting fat because they're eating too much of these unhealthy foods simply because of these foods' abundance therefore they would still be getting fat on nutritious, healthier foods if these foods' were equally abundant" is nothing more than a convenient hypothesis that has pretty much 0 basis in genetics or nutrition. This hypothesis also does nothing to explain the other few billion people who live in our current food-rich climate but still manage to stay lean with no effort on their part.

CS- I agree that the same could possibly be said for the low-fat diet, but "diet" is really the key word since I'm specifically interested in ad lib over decades, aka the way people really eat. LF ways of eating always involve restriction of calories, so yeah, if we take 200 kids and start half on LC and half on CR/LF and follow them for 25 years we would probably see equal incidence of metabolic derangement. Now let's say we run the same experiment with ad lib LF. This is mere speculation based on anecdotal experience, but I suspect the LF group would be crushing the LC in incidence of metabolic syndrome.

Additionally, what foods are you referring to by whole LC? If in regard to non-whole you're talking about those maltitol-loaded frankendesserts, then I would hesitate to call them LC let alone whole. And what exactly constitutes "processed crap" on LF? Snackwells are low-fat, low-protein and contain about half sugar and half enriched wheat flour, so therefore we should shun them? Artisan ciabatta and a little strawberry jam probably has the exact same nutritional profile but is acceptable? Because it's not processed? Too confusing for me.

Leo said: "But if for any reason LC and paleo foods became the cheap and abundant food that you can buy at any corned of the street, in any fast food, theaters, playground... then it would be the norm for people to become fat eating nothing but LC and paleo foods. That's because way more important than caloric density or type of food is cultural food abudancy."

Leo, I still highly doubt this is the whole truth.

http://www.ncbi.nlm.nih.gov/pubmed/19209185

This is a very small cross over study with only nine participants and no control group. But in my book large results in small groups ought to ring a bell. Apart from improving any health parameter you can think of, leaving out 'neolithic' items led to spontaneous undereating. Even crazier: the ivestigators had to force feed the participants more than 300 extra kcal per day in order to keep them weight stable on the 'paleo diet'.

The same phenomenon has been observed and documented by Lindeberg and, for what it's worth, I know several confirming anecdotes myself. Something in our food besides energy content (partly) controls our intake and even body composition (I don't say weight, although the mentioned experiment suggests such blasphemia).

Leo said: "But if for any reason LC and paleo foods became the cheap and abundant food that you can buy at any corned of the street, in any fast food, theaters, playground... then it would be the norm for people to become fat eating nothing but LC and paleo foods. That's because way more important than caloric density or type of food is cultural food abudancy."

Leo, I still highly doubt this.

http://www.ncbi.nlm.nih.gov/pubmed/19209185

This is a very small cross over study with only nine participants and no control group, but in my book large results in small groups ought to ring a bell. Apart from improving any health parameter you can think of, leaving out 'neolithic' items led to spontaneous undereating. Even crazier: the ivestigators had to force feed the participants with more than 300 extra kcal per day in order to keep them weight stable on the 'paleo diet'.

The same phenomenon has been observed and documented by Lindeberg and, for what it's worth, I know several confirming anecdotes myself. Something in our food besides energy content (partly) controls our intake and even body composition (I don't say weight, although the mentioned experiment suggests such blasphemia).

Sanjeev- pointing to the Kitavans and going "look! this set of HGs eats LF and they're lean" isn't evidence toward the experiment I described at all. HG cultures are also a very small subset of the human population that live in relative isolation and expend a large number of calories obtaining food (not to mention the Kitavans eat no refined grains and negligible sugar), so I could point to the LC Hadza or Inuit and it wouldn't support my point anymore than yours opposes it.

Regardless, my experiment with 200 kids was conceived with modern Western culture in mind, i.e. ad lib LC vs LF for kids whose parents shop in supermarkets rather than spend 8 hrs a day gathering coconuts and tubers.

Sanjeev- indeed, the Kitavans do consume somewhere around 10% of calories from fruit according to Stephan so that probably can't be called negligible. At the same time, 50g/day of fructose sourced from fiber-laden whole fruit in a physically active hunter-gatherer isn't exactly something to write home about.